Hemorrhagic pericarditis and pericardial tamponade occurring in the setting of acute myocardial infarction (MI) are very uncommon. Even rare is its presentation as acute liver failure. We describe a patient who presented with acute liver failure postangioplasty and stenting of left anterior descending and right coronary artery in the setting of a large transmural anterior wall MI. Acute liver failure in this case was attributable to a hemorrhagic pericardial effusion and tamponade. It completely resolved following pericardiocentesis. This unusual presentation of an unusual complication and its management is discussed.

Pericardial tamponade in the setting of acute myocardial infarction (MI) is a challenging problem. It can result either from a mechanical complication like cardiac rupture or from an interventional complication like coronary perforation. Very rarely, it can be secondary to hemorrhagic transformation of pericarditis in the setting of a large MI. We describe a rare case of hemorrhagic pericarditis complicating into pericardial tamponade and presenting as acute liver failure in a patient with a large anterior MI who was managed with dual-antiplatelet and glycoprotein IIb/IIIa inhibitor therapy eptifibatide along with double-vessel percutaneous transluminal coronary angioplasty.

Case Report

A 54-year-old-male, chronic smoker, presented with chest pain of 2 h duration. There was no previous history of hypertension or diabetes. Electrocardiogram revealed anterior wall ST elevation MI. His pulse rate was 90 beats per minute and blood pressure was 120/70 mmHg. Echocardiogram revealed left ventricular ejection fraction of 25% with a severely hypokinetic septum and anterior wall. There was no pericardial effusion. After giving 325 mg aspirin, 300 mg clopidogrel, and 40 mg atorvastatin, he was shifted to the cardiac catheterization laboratory. Coronary angiography revealed 95% thrombotic stenosis in the ectatic mid left anterior descending (LAD) artery [Figure 1]a and 80% ostioproximal stenosis in the right coronary artery (RCA) [Figure 1]b. We advised percutaneous transluminal coronary angioplasty (PTCA) and stenting to the LAD (culprit vessel). However, he declined any intervention and hence was instituted on glycoprotein (Gp) IIb/IIIa inhibitor eptifibatide and shifted to coronary care unit. He agreed for PTCA next day which was done uneventfully using two Yukon drug-eluting stents, one for the LAD [Figure 2]a and the other for the RCA [Figure 2]b in the same sitting, with a good result. On day 3 early morning, he complained of nausea and abdominal pain with two episodes of vomiting. The pulse rate was 110 beats per minute, and the blood pressure was 90 systolic. Physical examination revealed hepatomegaly, neck veins were not distended, and the heart sounds were normal. He was administered intravenous pantoprazole and ondansetron; however, due to the persistence of symptoms, further investigations in the form of abdominal ultrasonography, complete blood counts, liver function tests (LFTs), serum amylase, and lipase were done. His hemoglobin was found to be 11.1 gm% (reduced from 13.7 gm% at baseline). To our surprise, LFTs revealed very high transaminase levels. Total bilirubin was 1.7 mg% (normal range <1 mg%); direct bilirubin was 0.5 mg% (normal <0.6 mg%); serum glutamic oxaloacetic transaminase (SGOT) was 3958 IU/L (normal range up to 46); serum glutamic pyruvic transaminase (SGPT) was 2420 IU/L (normal range up to 49); alkaline phosphatase (ALP) was 106 IU/L (normal range 98–280); and lactate dehydrogenase (LDH) was 3911 (normal range: 235–470). Prothrombin time (PT) was 15.8 s against a control of 12.3 s; international normalized ratio was 1.38; blood urea was 50 mg% (baseline 16 mg%); and serum creatinine was 0.8 mg% (baseline 0.8 mg%). Total serum proteins were 5.7 g% (normal range: 6.7–8.7 gm%); serum albumin was 3.8 g% (normal range: 3.5–5 g%); and serum globulins was 1.9 g% (normal range: 2–3 g%). Ultrasound of the abdomen revealed a normal liver with patent hepatic vasculature and a normal gall bladder without stones or intrahepatic ductal dilatation, but a pericardial effusion was noted. Viral markers for hepatitis were negative. An echocardiogram at this stage revealed a large circumferential pericardial effusion of 2.2 cm, dilated inferior vena cava to 2.6 cm, and 25% respiratory variation in mitral inflow velocities, suggesting cardiac tamponade physiology without clinical features of tamponade [Figure 3]. Considering the hemodynamic instability and echocardiographic evidence of pericardial tamponade, immediate pericardiocentesis was done and 120 ml of hemorrhagic pericardial fluid was drained, leading to hemodynamic stabilization. Pigtail catheter was kept in the pericardial cavity for 2 days, and further 40 ml hemorrhagic fluid was aspirated. The patient was uneventfully discharged 3 days after pericardiocentesis. The echocardiogram revealed minimal pericardial effusion at discharge [Figure 4]. Liver functions normalized over the next 2 weeks. He is doing well at 4-year follow-up.

Our patient presented with features of acute liver failure in the form of nausea, vomiting, abdominal pain, and meteoric transaminitis after successful angioplasty. He also had tachycardia (heart rate 110 beats per minute) and hypotension (blood pressure 90 mmHg systolic) which we wrongly attributed to dehydration secondary to nausea and vomiting. Since the patient did not have any significant fresh ST-T changes, our attention was shifted to hepatitis as a cause for his symptoms. However, when we did a detailed echocardiogram following the ultrasound report suggesting pericardial effusion, we found a large pericardial effusion with tamponade which was not there to begin with. Pericardial effusion with tamponade presenting as acute liver failure is very uncommon but has been described in literature.[1] The most likely cause of the effusion in our patient was a hemorrhagic pericarditis transforming into cardiac tamponade since there was no coronary leak and no mechanical complication like cardiac rupture. The angiography images were carefully reviewed revealing no coronary leak. The review of the echocardiogram also did not reveal any evidence of myocardial rupture.

This complication possibly occurred in the presence of triple antiplatelet therapy (aspirin, clopidogrel, and eptifibatide). This is extremely uncommon. In the absence of thrombolysis, it is even more uncommon. Our patient had not been thrombolyzed. Hemorrhagic pericarditis has previously been described with dual-antiplatelet therapy in conjunction with abciximab and recent thrombolysis.[2] It has also been described with dual-antiplatelet therapy and abciximab in the setting of primary angioplasty.[3] We could not come across any report of this complication with eptifibatide. The clinical presentation of this unusual complication with nausea and vomiting and the biochemistry picture suggesting acute ischemic hepatitis (markedly elevated SGOT and SGPT) was even more unusual. Atrial tamponade leading to similar clinical presentation with acute liver failure has been described previously in a patient postcardiac surgery, but, to the best of our knowledge, there is no such presentation postangioplasty.[4]

In our setting, three possible explanations could explain this meteoric rise of transaminase-acute viral hepatitis, toxic hepatitis, or ischemic hepatitis. Negative serology ruled out acute viral hepatitis. Toxic hepatitis was also ruled out since there was no hepatotoxic drug used. Although statins can cause transaminitis, such a marked elevation of transaminases is extremely unlikely with statin use. Thus, our patient in all probability had acute ischemic hepatitis (hypoxic hepatitis or liver shock). The classic hepatic biochemical abnormalities and less severe signs of cholestasis and liver failure are the hallmarks of this condition. The typical biochemistry picture of a meteoric rise of SGOT/SGPT coupled with meteoric LDH rise and only mild elevation of bilirubin/PT/ALP further supports this diagnosis.[5] Furthermore, an early onset of renal insufficiency is rare in other forms of hepatitis, whereas it is quite common in ischemic hepatitis.[5] The mechanism is reduced hepatic blood flow and increased hepatic venous congestion causing centrilobular necrosis with little/no inflammation. The subsequent settlement of transaminitis with pericardiocentesis, absence of any ultrasonographic anomalies, and negative serology suggest hemorrhagic tamponade as the only cause. We have not come across this unusual presentation of pericardial tamponade as acute liver failure following angioplasty in the literature before. Since our patient presented with abdominal pain, nausea, and vomiting and did not have any clinical features of pericardial tamponade, we were misled to consider an abdominal cause for his presentation. We never suspected presentation of pericardial tamponade as acute liver failure until an extensive literature review was done.

Conclusion

Pericardial tamponade can arise in an acute MI setting even in the absence of a mechanical complication or coronary perforation. Hemorrhagic pericarditis can rapidly develop into tamponade rarely in the setting of antiplatelet therapy, especially if Gp IIb/IIIa inhibitors are used and the MI is large and transmural. We must be aware of this albeit rare possible complication in the setting of acute MI intervention.

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